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In two healthy and two diseased whitefish (Coregonus Wartmanni) taken from Lake Constance (FRG), ankylosis of the vertebral column was investigated both roentgenologically and histologically. Subsequent to the collapse and necrosis of the "residual" spinal cord within the intervertebral spaces, the outside edges of the vertebral bodies come into direct contact. The compression and tensile forces that occur to an increased extent as a result of the instability, lead not only to a remodelling of the vertebral bodies, but also to the formation of spondylotic osteophytes at the edges of the vertebrae and, as a result of periosteal stimulation, to the development of cellular hyaline cartilage, which fills the intervertebral spaces. Finally, as a result of perichondral ossification, a bony ankylosis develops. The humping of the spine of the fish due to the stiffening and shortening of the vertebral column, is accompanied by a restriction in the animal's freedom of movement. Muscular atrophic processes and disordered food uptake give rise to poor growth and a reduction in the weight of the diseased fish. These remodelling processes in the spine resulting from instability are specific to the periosteum and may be equated with the changes seen in man in spondylosis deformans. The possible cause of this vertebral column ankylosis is cadmium poisoning. The accumulation of this heavy metal obviously leads primarily to an irreversible toxic degeneration of the cells of the chorda dorsalis.
The paper reviews various classifications and surgical techniques for the treatment of temporomandibular joint ankylosis. PubMed, EBSCO, Web of Science, and Google Scholar were searched using a combination of keywords. Articles related to classification, resection-reconstruction of the temporomandibular joint, and management of airway obstruction were considered and categorized based on the objectives. Seventy-nine articles were selected, which included randomized clinical trials, non-randomized controlled cohort studies, and case series. Though several classifications exist, most classifications are centered on the radiographic extent of the ankylotic mass and do not include the clinical and functional parameters. Hence there is a need for a comprehensive staging system that takes into consideration the age of the patient, severity of the disease, clinical, functional, and radiographic findings. Staging the disease will help the clinician to adopt a holistic approach in treating these patients. Interpositional arthroplasty (IA) results in better maximal incisal opening compared with gap arthroplasty, with no significant difference in recurrent rates. Distraction osteogenesis (DO) is emerging as a popular technique for the restoration of symmetry and function as well as for relieving airway obstruction. IA, with a costochondral graft, is recommended in growing patients and may be combined with or preceded by DO in cases of severe airway obstruction. Alloplastic total joint replacement combined with fat grafts and simultaneous osteotomy procedures are gaining popularity. A custom-made total joint prosthesis using CAD/CAM can efficiently overcome the shortcomings of stock prostheses.
Mutations in the progressive ankylosis protein (NP_473368, human ANKH) cause craniometaphyseal dysplasia (CMD), characterized by progressive thickening of craniofacial bones and widened metaphyses in long bones. The pathogenesis of CMD remains largely unknown, and treatment for CMD is limited to surgical intervention. We have reported that knock-in mice (AnkKI/KI) carrying a F377del mutation in ANK (NM_020332, mouse ANK) replicate many features of CMD. Interestingly, ablation of the Ank gene in AnkKO/KO mice also leads to several CMD-like phenotypes. Mutations causing CMD led to decreased steady-state levels of ANK/ANKH protein due to rapid degradation. While wild type (wt) ANK was mostly associated with plasma membranes, endoplasmic reticulum (ER), Golgi apparatus and lysosomes, CMD-linked mutant ANK was aberrantly localized in cytoplasm. Inhibitors of proteasomal degradation significantly restored levels of overexpressed mutant ANK, whereas endogenous CMD-mutant ANK/ANKH levels were more strongly increased by inhibitors of lysosomal degradation. However, these inhibitors do not correct the mislocalization of mutant ANK. Co-expressing wt and CMD-mutant ANK in cells showed that CMD-mutant ANK does not negatively affect wt ANK expression and localization, and vice versa. In conclusion, our finding that CMD mutant ANK/ANKH protein is short-lived and mislocalized in cells may be part of the CMD pathogenesis.
Gap arthroplasty (GA) and interpositional arthroplasty (IA) are widely used for the treatment of temporomandibular joint ankylosis (TMJA). However, controversy remains as to whether IA is superior to GA. PubMed, EMBASE, the Cochrane Library, the Web of science and the China National Knowledge Infrastructure were searched for literature regarding these procedures (published from 1946 to July 28, 2014). A study was included in this analysis if it was: (1) a randomized controlled trial or non-randomized observational cohort study; (2) comparing the clinical outcomes between GA and IA with respect to the maximal incisal opening (MIO) and reankylosis; (3) with a follow-up period of at least 12 months. The methodological quality of the included studies was evaluated according to the Newcastle-Ottawa Scale Eight non-randomized observational cohort studies with 272 patients were included. All the statistical analyses were performed using the RevMan 5.3 and Stat 12. The pooled analysis showed no significant difference in the incidence of reankylosis between the IA group (13/120) and the GA group (29/163) (RR= 0.67, 95% CI=0.38 to 1.16; Z=1.43, p=0.15). The IA group showed a significantly larger MIO than the GA group (MD=1.96, 95% CI=0.21 to 3.72, Z=2.19, p=0.03, I(2)=0%). In conclusion, patients with TMJA could benefit more from IA than GA, with a larger MIO and a similar incidence of reankylosis. IA shows to be an adequate option in the treatment of TMJA based on the results of maximal incisal opening.
The progressive ankylosis gene (ank) encodes a transmembrane protein that transports intracellular inorganic pyrophosphate (PP(i)) to the extracellular milieu. ank/ank mice, which express a truncated nonfunctional ANK, showed a markedly reduced bone mass, bone-formation rate, and number of tartrate-resistant acid phosphatase-positive (TRAP(+)) multinucleated osteoclasts. ANK function deficiency suppressed osteoblastic differentiation of ank/ank bone marrow stromal cells, as indicated by the decrease in the expression of bone marker genes, including osterix, reduced alkaline phosphatase activity, and mineralization. Runx2 gene expression levels were not altered. Conversely, overexpression of ANK in the preosteoblastic cell line MC3T3-E1 resulted in increased expression of bone marker genes, including osterix. Whereas runx2 expression was not altered in ANK-overexpressing MC3T3-E1 cells, runx2 transcriptional activity was increased. Extracellular PP(i) or P(i) stimulated osteoblastogenic differentiation of MC3T3-E1 cells or partially rescued delayed osteoblastogenic differentiation of ank/ank bone marrow stromal cells. A loss of PP(i) transport function ANK mutation also stimulated osteoblastogenic differentiation of MC3T3-E1 cells. Furthermore, ANK function deficiency suppressed the formation of multinucleated osteoclasts from ank/ank bone marrow cells cultured in the presence of macrophage colony-stimulating factor and receptor activator of nuclear factor-kappaB ligand. In conclusion, ANK is a positive regulator of osteoblastic and osteoclastic differentiation events toward a mature osteoblastic and osteoclastic phenotype.
The purpose of this study was to compare the clinical outcomes of ultrasonic surgery to the conventional bone cutting technique using bur and saw for the release of ankylosis of temporomandibular joint. We conducted a prospective cohort study on 25 patients with 38 ankylotic joints at Chinese PLA General Hospital from March 01, 2012 to March 01, 2016. Patients were followed up at least 2 years postoperatively. The primary outcome was the intraoperative blood loss per joint. The secondary outcome was the long-term (≥2 years) improvement of maximum mouth opening. The blood loss was significantly reduced in the ultrasonic group compared to the conventional group (107.3 ± 62.3 ml vs. 186.3 ± 92.6 ml, P = 0.019). The long-term improvements of maximum mouth opening were substantial and stable in both groups (33.5 ± 4.8 mm in the ultrasonic group vs. 29.2 ± 6 mm in the conventional group, P = 0.06). Multivariate linear regression analysis showed a significant association between blood loss and technique used (coefficient: 66.3, 95% confidence interval: 22.1,110.4, P = 0.006). The ultrasonic surgery was associated with less intraoperative blood loss when compared to the conventional method for the release of ankylosis of temporomandibular joint while providing a stable and comparable long-term improvement of maximum mouth opening.
Ankylosis spondylitis (AS) is a disease mainly characterized by sacroiliac joint and spinal attachment point inflammation. Long non-coding RNA (lncRNA) plays a key role in the progression of many diseases. However, few studies have been conducted on the function of lncRNA maternally expressed gene 3 (MEG3) in AS. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the relative levels of MEG3, microRNA let-7i, sclerostin (SOST), and inflammatory cytokines. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and biotin-labeled RNA pull-down assay were used to confirm the interaction between MEG3 and let-7i or let-7i and SOST. In addition, western blot (WB) analysis was performed to detect the protein levels of osteogenesis markers and SOST. The expression levels of MEG3 and SOST were decreased and let-7i was increased in AS patients. MEG3 could interact with let-7i in AS fibroblasts, and let-7i overexpression reversed the suppressive effect of MEG3 upregulation on the inflammation and bone formation of AS. Additionally, let-7i could target SOST, and SOST silencing reversed the inhibitory effect of let-7i inhibitor or MEG3 overexpression on the inflammation and bone formation of AS. Furthermore, SOST expression was positively regulated by MEG3, while was negatively regulated by let-7i. Our results revealed that lncRNA MEG3 promoted SOST expression to restrain the progression of AS by sponging let-7i, which provided a treatment target for AS.
Temporomandibular joint (TMJ) ankylosis is an uncommon clinical entity in human and veterinary medicine. However, the condition is severely debilitating and is life-limiting if not treated. This study sought to characterize the intra- and extra-articular features of naturally occurring TMJ ankylosis in cats. TMJs from client-owned cats (n = 5) that underwent bilateral TMJ gap arthroplasty were examined and compared with TMJs from healthy, age-matched feline cadavers (n = 2) by cone-beam computed tomography (CBCT), micro-computed tomography (μCT) and histologically. Features of bilateral intra- and extra-articular ankylosis compounded by degenerative joint lesions were identified radiographically and histologically in all affected cats. Features of TMJ 'true' ankylosis included variable intracapsular fibro-osseous bridging, degeneration of the disc and the articular surfaces, narrowing of the joint space and flattening of the condylar process of the mandible. Extra-articular features of TMJ ankylosis included periarticular bone formation and fibro-osseous bridging between the mandible, zygomatic arch and coronoid process. In addition, subchondral bone loss or sclerosis, irregular and altered joint contours and irregularly increased density of the medullary bone characterized the degenerative changes of the osseous components of the TMJ. Complex radiological and histological features of both ankylosis and pseudoankylosis were identified that clinically manifested in complete inability to open the mouth.
Vascular calcification is a major risk factor of cardiovascular mortality, particularly for patients with end-stage renal disease and diabetes. Although chronic inflammation is one of the etiologic factors, the underlying mechanism is not fully understood. To clarify this, we studied how nuclear factor-kappa B (NF-κB) induction, a mediator of inflammation, might promote vascular calcification. Activation of NF-κB by tumor necrosis factor (TNF) promoted inorganic phosphate-induced calcification in human aortic smooth muscle cells. Pyrophosphate (an inhibitor of calcification) efflux to the extracellular matrix was suppressed along with the decreased expression of ankylosis protein homolog (ANKH), a transmembrane protein that controls pyrophosphate efflux of cells. The restoration of ANKH expression in these cells overcame the decreased pyrophosphate efflux and calcification. Tristetraprolin, a downstream product of NF-κB activation, may mediate destabilization of ANKH mRNA as its knockdown by shRNA increased ANKH expression and decreased calcification. Furthermore, a rat chronic renal failure model, with increased serum TNF levels, activated NF-κB and decreased ANKH levels. In contrast, the inhibition of NF-κB maintained ANKH expression and attenuated vascular calcification both in vivo and in vitro. Both human calcified atherosclerotic lesions and arteries from patients with chronic kidney disease had activated NF-κB and decreased ANKH expression. Thus, TNF-activated NF-κB promotes inflammation-accelerated vascular calcification by inhibiting ankylosis protein homolog expression and consequent pyrophosphate secretion.
To prevent spinal progression in ankylosing spondylitis, initiating TNF-inhibitor treatment as early as possible is suggested. However, the outcomes are inconsistent in previous clinical studies. Here, we investigated the effect of TNF inhibition alone on spinal progression when used during arthritis development in a murine model. We injected 8-week-old SKG mice with curdlan (curdlan group). We injected adalimumab at 3 and 9 weeks after the first curdlan injection (ADA group). The clinical scores of peripheral arthritis decreased in the ADA group at 3 weeks after first adalimumab injection. Using positron emission tomography-magnetic resonance imaging and histologic examination, spinal inflammation was observed in the curdlan group, and was significantly deceased in the ADA group. However, spinal osteoblast activities by imaging using OsteoSense 680 EX and bone metabolism-related cytokines such as receptor activator of nuclear factor-kappa B ligand, osteoprotegerin, Dickkopf-1, and sclerostin levels except IL-17A level were not different between the two groups. We conclude that treating TNF inhibitor alone reduced peripheral arthritis score and spinal inflammation in curdlan-injected SKG mice but did not decrease the spinal osteoblast activity, suggesting little effect on spinal ankylosis.
This study aimed to describe the clinical features of different types of traumatic temporomandibular joint (TMJ) ankylosis. Seventy-one patients with 102 ankylosed joints were retrospectively reviewed and categorized into four groups according to the grades of severity: type I, non-bony ankylosis of the joint with almost-normal joint space; type II, lateral bony ankylosis marked by a normal joint space that coexists with a radiolucent line; type III, complete bony ankylosis of the joint characterized by only a radiolucent line; and type IV, extensive bony ankylosis without any radiolucent line. The period of ankylosis, maximal mouth opening (MMO), rate of complications, and histopathological changes were compared among groups. Intergroup comparison showed significant differences in the clinical features of MMO and the incidence of complications (p < 0.05). Younger trauma patients tended to develop more severe types of ankylosis than older patients. Additionally, long post-trauma periods were related to the development of severe ankylosis. MMO was highly negatively correlated with the severity of ankylosis. Significant differences were noted among the four types of ankylosis. Younger trauma patients with long post-trauma periods tended to develop more severe TMJ ankylosis, experience more complications, and face more challenges in treatment than older patients.
Ankylosis is a physically and psychologically distressing condition to a patient. The aim of this study was to evaluate the efficiency of custom-made temporomandibular joint (TMJ) prosthesis (fossa-condyle component) in patients with unilateral ankylosis in restoring the form and functions of the TMJ.
Little is known about the mechanisms underlying the clinical overlap between gut inflammation and joint ankylosis, as exemplified by the concurrence of inflammatory bowel diseases (IBD) and ankylosing spondylitis (AS). As dysbiosis may serve as a common contributor, the anti-microbial pleiotropic factor lipocalin 2 could be a potential mediator due to its roles in inflammation and bone homeostasis.
The aim of this study was to compare the functional characteristics of mesenchymal stromal cells (MSCs) from a sheep model of traumatic temporomandibular joint (TMJ) fibrous and bony ankylosis. A sheep model of bilateral TMJ trauma-induced fibrous ankylosis on one side and bony ankylosis on the contralateral side was used. MSCs from fibrous ankylosed callus (FA-MSCs) or bony ankylosed callus (BA-MSCs) at weeks 1, 2, 4, and 8 after surgery were isolated and cultured. MSCs derived from the bone marrow of the mandibular condyle (BM-MSCs) were used as controls. The MSCs from the different sources were characterized morphologically, phenotypically, and functionally. Adherence and trilineage differentiation potential were presented in the ovine MSCs. These cell populations highly positively expressed MSC-associated specific markers, namely CD29, CD44, and CD166, but lacked CD31 and CD45 expressions. The BA-MSCs had higher clonogenic and proliferative potentials than the FA-MSCs. The BA-MSCs also showed higher osteogenic and chondrogenic potentials, but lower adipogenic capacity than the FA-MSCs. In addition, the BA-MSCs demonstrated higher chondrogenic, but lower osteogenic capacity than the BM-MSCs. Our study suggests that inhibition of the osteogenic and chondrogenic differentiations of MSCs might be a promising strategy for preventing bony ankylosis in the future.
Studies in the spontaneous ankylosis model in aging male DBA/1 mice and in patients with ankylosing spondylitis provide evidence that inflammation and new tissue formation leading to joint or spine ankylosis are likely linked but largely uncoupled processes. We previously proposed the 'entheseal stress' hypothesis that defines microdamage or cell stress in the enthesis as a trigger for these disease processes. Here, we further investigated the relationship between inflammation and ankylosis by focusing on the early phase of the spontaneous arthritis model.
Ankylosis progressive homolog (ANKH) is associated with fibroblast ossification in ankylosing spondylitis (AS). As the human ANKH gene is poorly characterized relative to its murine counterpart, the aim of the present study was to examine ANKH expression in ligament tissue isolated from patients with AS and the role played by this gene in AS‑associated fibroblast ossification. Fibroblasts were isolated from ligament tissue collected from patients with AS and ligament tissue from individuals with spinal cord fractures, then cultured. Fibroblasts from patients with AS were subsequently transfected with an ANKH overexpression vector, while those collected from individuals with spinal cord fractures were transfected with small interfering RNA specific for ANKH. Cell viability, apoptosis and mineralization were analyzed using MTT assays, flow cytometry and Alizarin Red staining, respectively. Furthermore, ANKH mRNA and protein expression levels were analyzed using reverse transcription‑quantitative PCR and western blotting analysis, respectively. The expression levels of osteogenesis markers, including alkaline phosphatase, osteocalcin, Runt‑related transcription factor 2, c‑Myc, as well as the β‑catenin signaling protein, were also determined using western blotting. The results of the present study revealed that ANKH protein expression levels were downregulated in AS total ligament tissue extract, compared with spinal fracture ligament. Moreover, the fibroblasts derived from patients with AS exhibited an increased viability and reduced apoptosis rates, compared with the fibroblasts from patients with spinal fracture. Notably, ANKH overexpression inhibited viability, mineralization and ossification, increased the phosphorylation of β‑catenin and downregulated β‑catenin and c‑Myc protein expression levels in fibroblasts from patients with AS. In addition, ANKH overexpression increased the ratio of p‑β‑catenin/β‑catenin in fibroblasts from patients with AS. By contrast, ANKH silencing in fibroblasts from patients with spinal fracture resulted in the opposite effect. In conclusion, the findings of the present study suggested that ANKH may inhibit fibroblast viability, mineralization and ossification, possibly by regulating the Wnt/β‑catenin signaling pathway.
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